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Associate Professor M.A. in Medical Sciences, Graduate Program Director Ph.D. 1992, Indiana University Plant Genetics and Development Phone: 773.508.3367 Fax: 773.508.3646 E-mail: fpicket@luc.edu 1999 Paper Ranks 12th. Out Of 50 Most-Frequently Cited Genetics Articles

RESEARCH INTERESTS

The shoot apical meristem of higher plants acts similarly to animal embryos, providing stem cells for organization into tissues and organs. My laboratory uses a genetic approach to identify mutations in the plant Arabidopsis thaliana which perturb the function of the shoot apical meristem. Since organ production is the main job of the meristem, we have screened for temperature sensitive mutations that fail to produce new leaves and other organs following germination.

Three mutations with strict developmental arrests at high temperature have been identified to date. I have designated these mutations arrested development (add)1, 2, and 3. Current and future projects include the molecular cloning of the ADD1 gene because this mutation was induced by the disruption of the gene by insertion of foreign DNA. This "DNA tag" has been used to isolate genomic DNA near the point of insertion and has facilitated the molecular characterization of the ADD1 region. The biochemical characterization of this gene will help shed light on the molecular mechanism of plant meristem function.

My laboratory is also producing fate maps of the apical region of the early Arabidopsis embryo to help chart the developmental programming of embryonic cells. Our fate mapping approaches use novel, transgenic lines to create sub-populations of cells in the early embryo with unique genotypes and phenotypes. The potential of early cells to contribute to later organs is scored by allowing embryos to complete development and growth into mature plants. Statistical modeling used to analyze the patterns of cell proliferation in many hundreds of plants has generated maps that demonstrate for the first time that developmental regulation in young plant embryos starts during very early cell divisions. These maps have helped us design new genetic screens that promise to generate unique new mutant types.

REPRESENTATIVE PUBLICATIONS

Force, A., W. A. Cresko, F. B. Pickett, S. R. Proulx, C. Amemiya, and M. Lynch. 2005. The origin of subfunctions and modular gene regulation. Genetics 170:433-446.

Force, A., Cresko, W.F. and Pickett, F.B. (2004). Informational accretion, gene duplication, and the mechanisms of genetic module parcellation. in Modularity in Development and Evolution: G. Schlosser and G. Wagner, Eds. University of Chicago Press.

Prince, V.E. and Pickett, F.B. (2002). Splitting Pairs: Diverging fates of duplicated genes. Nature Reviews: Genetics. 3: 827-837 .

Saulsberry, A., Martin, P.R., O'Brien, T., Sieburth, L.E. and Pickett, F.B. (2002). The induced sector Arabidopsis apical embryonic fate map. Development 129: 3403-3410.

Woodrick, R., Martin, P. R., Birman,I., and Pickett, F.B. (2000) The Arabidopsis Embryonic Shoot Fate Map . Development 127:813-820.

Force, A., Lynch, M., Pickett, F. B., Amores, A., Yan, Y-L and Postlethwait, J. (1999). Preservation of Duplicate Genes by Complementary, Degenerative Mutations. Genetics 151: 1531-1545 PDF of Paper

Leyser, H.M.O., Pickett, F.B., Dharmaseri, S., and Estelle, M. (1996). Mutations in the AXR3 Gene of Arabidopsis Result in Altered Auxin Response. The Plant Journal, 10: 403-413.

Pickett, F.B., Champagne, M.M. and Meeks-Wagner, D.R., (1996). Temperature-Sensitive Mutations that Arrest Arabidopsis Shoot Development. Development 122, 3799-3807.

Pickett, F.B. and Meeks-Wagner, D.R., (1995). Seeing Double: Appreciating Genetic Redundancy. The Plant Cell 7: 1347-1356.

Timpte, C., Lincoln, C., Pickett, F.B., Turner, J., and Estelle, M., (1995). The AXR1 and AUX1 Genes of Arabidopsis Function in Separate Auxin Responsive Pathways. The Plant Journal, 8: 561-569.

Fig. Wild-type and mutant seedling development after germination and growth at 29oC for 6 days. (A) Wild-type Wassilewskija seedling with cotyledons and two true leaves. The apical region of an arrested development 1 (add1) seedling lacking true leaves (B). Wild-type Landsberg erecta seedling (C) with an epicotyl displaying the first 2 true leaves. Both leaves have developed leaf blades and trichomes. (D) arrested development 2 seedling with cotyledons, true primordia are not visible.